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Abstract
Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the approximately 30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators-released by brain cells and peripheral immune cells-in both the origin of individual seizures and the epileptogenic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis.
Highlights
Epilepsy is a brain disorder characterized by an enduring predisposition to generate seizures, and by emotional and cognitive dysfunction.[1]
Despite the availability of a wide range of antiepileptic drugs (AEDs), about one-third of individuals with epilepsy still experience seizures that do not respond to medication.[2]
Catastrophic epilepsy can result from autoimmune brain processes; for example, Rasmussen encephalitis—a devastating catastrophic epilepsy of childhood that leads to hemibrain atrophy, hemiparesis and progressively severe seizures—has been linked to the presence of autoantibodies, including glutamate receptor 3 antibodies, these antibodies are not present in all cases.[52,53,54]
Summary
Epilepsy is a brain disorder characterized by an enduring predisposition to generate seizures, and by emotional and cognitive dysfunction.[1]. Clinical evidence for an important causal role for autoimmune disorders as triggers for seizures and epilepsy has emerged in several contexts Identifiable autoimmune disorders such as systemic lupus, vasculitis, multiple sclerosis, and paraneoplastic syndromes can all cause recurrent seizures.[51] catastrophic epilepsy can result from autoimmune brain processes; for example, Rasmussen encephalitis—a devastating catastrophic epilepsy of childhood that leads to hemibrain atrophy, hemiparesis and progressively severe seizures—has been linked to the presence of autoantibodies, including glutamate receptor 3 antibodies, these antibodies are not present in all cases.[52,53,54] Brains of individuals affected by Rasmussen encephalitis contain reactive astrocytosis, activated microglial cells and proinflammatory mediators, and are infiltrated by lymphocytes.[8,55,56,57,58,59] Catastrophic epilepsy has been associated with other disorders in which auto antibodies attack brain tissue. The authors of this review concluded that, at present, no evidence exists to support either the safety or the efficacy of ACTH for general pediatric epilepsies.[173]
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